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Myocardial infarction



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Myocardial infarction

  1. 1. Acute Myocardial Infarction Sarah Priore RN BSN
  2. 2. Objectives <ul><ul><li>Define and understand the epidemiology of MI’s and how they are classified </li></ul></ul><ul><ul><li>Will be able to identify the risk factors associated with MI’s </li></ul></ul><ul><ul><li>Will be able to recognize signs and symptoms of acute MI and what the appropriate interventions are. </li></ul></ul><ul><ul><li>Understand the treatment options available to treat acute MI. </li></ul></ul>
  3. 3. Definition <ul><li>Otherwise know as heart attack </li></ul><ul><li>An MI occurs when there is a diminished blood supply to the heart which leads to myocardial cell damage and ischemia. </li></ul><ul><li>Contractile function stops in the necrotic areas of the heart. </li></ul><ul><li>Ischemia usually occurs due to blockage of the coronary vessels. </li></ul>
  4. 4. Definition cont. <ul><li>This blockage is often the result of thrombus that is superimposed on an ulcerated or unstable atherosclerotic plaque formation in the coronary artery. </li></ul><ul><li>MI’s are described by the area of occurrence. </li></ul><ul><li>Anterior, Inferior, Lateral or Posterior. </li></ul>
  5. 5. Coronary Artery Anatomy
  6. 6. Coronary artery events <ul><li>Ischemia – Outer most area, source of arrhythmias, viable if no further infarction. </li></ul><ul><li>Injury – Viable tissue found between ischemic and infarcted areas. </li></ul><ul><li>Infarction/necrosis – Center area, dead not viable tissue that turn into scar. </li></ul>
  7. 9. MI Classifications <ul><li>MI’s can be subcategorized by anatomy and clinical diagnostic information. </li></ul><ul><li>Anatomic </li></ul><ul><li>Transmural and Subendocardial </li></ul><ul><li>Diagnostic </li></ul><ul><li>ST elevations (STEMI) and non ST elevations (NSTEMI). </li></ul>
  8. 10. Epidemiology <ul><li>MI’s are the leading cause of death in the United States, affecting one in five men and one in six women. </li></ul><ul><li>450,000 people in the US die from coronary disease each year. </li></ul><ul><li>Incidence rates increase with age as do mortality rates due to infarction. </li></ul>
  9. 11. Epidemiology <ul><li>The survival rate for those hospitalized due to MI has reached approximately 95%. </li></ul><ul><li>This is the result of the advancements made in modern medical technology. </li></ul>
  10. 12. Risk Factors <ul><li>The presence of any risk factor is associated with doubling the risk of an MI. </li></ul><ul><li>Non Modifiable </li></ul><ul><li>Age </li></ul><ul><li>Gender </li></ul><ul><li>Family history </li></ul>
  11. 13. Risk Factors <ul><li>Modifiable </li></ul><ul><li>Smoking </li></ul><ul><li>Diabetes Control </li></ul><ul><li>Hypertension </li></ul><ul><li>Hyperlipidemia </li></ul><ul><li>Obesity </li></ul><ul><li>Physical Inactivity </li></ul>
  12. 14. Smoking <ul><li>Tobacco use increases the risk of coronary artery disease two to six times more than non smokers. </li></ul><ul><li>Nicotine increases platelet thrombus adhesion and vessel </li></ul><ul><li>inflammation. </li></ul>
  13. 15. Diabetes & Hypertension <ul><li>Diabetes not only increases the rate of atherosclerotic formation in vascular vessels but also at an earlier age. </li></ul><ul><li>The constant stress of high blood pressure has been associated with the increased rate of plaque formation. </li></ul><ul><li>Shearing Stress and inflammation of endothelial lining begins the process. </li></ul>
  14. 16. Hyperlipidemia <ul><li>Elevated levels of cholesterol, LDL’s or triglycerides are associated with the increased risk of coronary plaque formation and MI. </li></ul><ul><li>Almost 50% of the U.S. </li></ul><ul><li>population has some </li></ul><ul><li>form of dyslipidemia. </li></ul>
  15. 17. Obesity and Physical Inactivity <ul><li>Mortality rate from CAD is higher in those who are obese. </li></ul><ul><li>Some evidence shows that those who carry their weight in their abdomen have a higher incidence of CAD </li></ul><ul><li>Physically inactive people have lower HDL levels with higher LDL levels and an increase in clot formation. </li></ul>
  16. 18. Pathophysiology <ul><li>Ischemia develops when there is an increased demand for oxygen or a decreased supply of oxygen. </li></ul><ul><li>Ischemia can develop within 10 seconds and if it lasts longer than 20 minutes, irreversible cell and tissue death occurs. </li></ul><ul><li>Myocardial cell death begins at the endocardium. The area most distal to the arterial blood supply. </li></ul>
  17. 19. Pathophysiology <ul><li>As vessel occlusion continues cell death spreads to the myocardium and eventually to the epicardium. </li></ul><ul><li>Severity of the MI depends on three factors. </li></ul><ul><ul><li>Level of occlusion </li></ul></ul><ul><ul><li>Length of time of occlusion </li></ul></ul><ul><ul><li>Presence or absence of collateral circulation </li></ul></ul>
  18. 20. Signs and Symptoms <ul><li>Signs and symptoms are unique to each individual patient. </li></ul><ul><li>Ranging from no symptoms to sudden cardiac arrest. </li></ul>
  19. 21. Chest Pain <ul><li>The most common initial manifestation is chest pain or discomfort. </li></ul><ul><li>This is not relieved by rest, position change or nitrate administration. </li></ul><ul><li>Pain is described by heaviness, pressure, fullness and crushing sensation. </li></ul><ul><li>Not everyone experiences this sensation. </li></ul>
  20. 22. Chest Pain <ul><li>PQRST assessment for chest pain </li></ul><ul><li>P- Precipitating events </li></ul><ul><li>Q- Quality of pain </li></ul><ul><li>R- Radiation of pain </li></ul><ul><li>S- Severity of pain </li></ul><ul><li>T- Timing </li></ul>
  21. 23. Nausea and Vomiting <ul><li>Not everyone will experience this. </li></ul><ul><li>Vomiting results as a reflex from severe pain. </li></ul><ul><li>Vasovagal reflexes initiated from area of ischemia. </li></ul>
  22. 24. Sympathetic Nervous System Stimulation <ul><li>During an MI increased catecholamines are released. </li></ul><ul><li>This results in diaphoresis and vasoconstriction of peripheral blood vessels. </li></ul><ul><li>“ Cool Sweat” with a temperature increase during the first 24 hours. </li></ul>
  23. 25. Cardiovascular Changes <ul><li>Initially the BP and pulse may be elevated. </li></ul><ul><li>Later, BP will drop due to decreased cardiac output. </li></ul><ul><li>Urine output will decrease </li></ul><ul><li>Lung sounds will change to crackles </li></ul><ul><li>Jugular veins may become distended and have obvious pulsations. </li></ul>
  24. 26. Video <ul><li>Watch your own heart attack…This is a little graphic! </li></ul><ul><li> </li></ul>
  25. 27. Within the first 10 minutes upon arrival to the hospital: <ul><li>Check vital signs and evaluate oxygen saturation </li></ul><ul><li>Establish IV access </li></ul><ul><li>Obtain and review 12-lead ECG </li></ul><ul><li>Take a brief focused history and perform a physical exam </li></ul><ul><li>Obtain blood samples to evaluate initial cardiac markers, electrolytes and coagulation </li></ul>
  26. 28. Diagnostics <ul><li>After collecting patient health history, a series of EKG’s should be taken to rule out or confirm MI. </li></ul><ul><li>12 lead EKG’s can help to distinguish between ST-elevation MI’s and Non-ST-elevation MI’s. </li></ul>
  27. 29. Normal Sinus Rhythm
  28. 30. Angina <ul><li>Stable </li></ul><ul><li>Chest pain caused by the build up of lactic acid and irritation to the myocardial nerve fibers. </li></ul><ul><li>Chest pain caused by the 4 E’s. </li></ul><ul><li>Pain is usually relieved with rest, pain meds and nitrates. </li></ul>
  29. 31. Variable/Prinzmetal/Spasm <ul><li>Transient ischemia that occurs unpredictably and almost always at rest. </li></ul><ul><li>Pain is caused by vasospasm of the arteries. </li></ul><ul><li>ST segment elevations will be noted. </li></ul>
  30. 32. Unstable <ul><li>Chest pain at rest or with exercise and tends to last greater than 15 minutes. </li></ul><ul><li>This results in reversible myocardial ischemia but is a sign that an infarct is soon to come. </li></ul><ul><li>EKG will reveal ST segment depression and T wave inversion. </li></ul>
  31. 33. STEMI <ul><li>ST segment elevations </li></ul><ul><li>T wave changes </li></ul><ul><li>Q wave development </li></ul><ul><li>Enzyme elevations </li></ul><ul><li>Reciprocals </li></ul>
  32. 34. NSTEMI <ul><li>ST segment depressions </li></ul><ul><li>T wave changes </li></ul><ul><li>No Q wave development </li></ul><ul><li>Mild enzyme elevations </li></ul><ul><li>No reciprocals </li></ul>
  33. 35. STEMI vs. NSTEMI
  34. 36. Phases of a STEMI <ul><li>Hyperacute Phase </li></ul><ul><ul><li>Occurs within the first few hours of MI onset. </li></ul></ul><ul><ul><li>Leads facing the infarcted surface: ST segment elevation. </li></ul></ul><ul><ul><li>Leads facing the uninjured surface: ST segment depression (reciprocals) </li></ul></ul><ul><ul><li>T waves become tall, widened and might be taller than the R wave. </li></ul></ul>
  35. 37. Phases of a STEMI <ul><li>Fully Evolved Phase </li></ul><ul><ul><li>Q wave development </li></ul></ul><ul><ul><li>ST elevation </li></ul></ul><ul><ul><li>T waves start to become inverted in leads facing the injury. </li></ul></ul>
  36. 38. Phases of a STEMI <ul><li>Resolution phase </li></ul><ul><ul><li>Weeks after there will be a gradual return of ST segments to baseline. </li></ul></ul><ul><ul><li>T waves will gradually return to normal but are the last to change back. </li></ul></ul>
  37. 39. Serum Cardiac Markers <ul><li>Myocardial cells produce certain proteins and enzymes associated with cellular functions. </li></ul><ul><li>When cell death occurs, these cellular enzymes are released into the blood stream. </li></ul><ul><li>CPK and troponin </li></ul>
  38. 40. CPK <ul><li>Creatine Phosphokinase </li></ul><ul><li>Begin to rise 3 to 12 hours after acute MI. </li></ul><ul><li>Peak in 24 hours </li></ul><ul><li>Return to normal in 2 to 3 days </li></ul>
  39. 41. Troponin <ul><li>Myocardial muscle protein released into circulation after injury. </li></ul><ul><li>These are highly specific indicators of MI. </li></ul><ul><li>Troponin rises quickly like CK but will continue to stay elevated for 2 weeks. </li></ul><ul><li>Myoglobin-lacks cardiac specificity. </li></ul>
  40. 42. Serum Cardiac Markers
  41. 43. Treatment Options <ul><li>The immediate goal for any acute MI is to restore normal coronary blood flow to vessels and salvage myocardium. </li></ul><ul><li>There are a variety of medical and medicinal therapies to treat an MI. </li></ul>
  42. 44. General Treatment for the MI patient <ul><li>MONA </li></ul><ul><li>Morphine </li></ul><ul><li>Oxygen </li></ul><ul><li>Nitroglycerin </li></ul><ul><li>Aspirin </li></ul>
  43. 45. Fibrinolytic Therapy <ul><li>Indicated for patients with STEMI MI’s. </li></ul><ul><li>Should be given within 12 hours of symptom onset. </li></ul><ul><li>Fibrinolytics will break down clots found within the vessles </li></ul><ul><li>Contraindications: post op surgical patients, history of hemorrhagic stroke, ulcer disease, pregnancy, ect. </li></ul>
  44. 46. Cardiac Catheterization <ul><li>A diagnostic angiography which includes angioplasty and possible stenting. </li></ul><ul><li>Performed by an interventional cardiologist with a cardiac surgeon on stand by. </li></ul><ul><li>Percutaneous procedure through the femoral or brachial artery. </li></ul>
  45. 47. Cardiac Catheterization <ul><li>Upon arrival to the cath lab all actue MI patients will receive: </li></ul><ul><ul><li>A bolus dose of plavix </li></ul></ul><ul><ul><li>IV Integrelin </li></ul></ul><ul><ul><li>Heparin dose either subcu or IV drip </li></ul></ul><ul><ul><li>Angiomax : a DTI may be substituted for heparin and integrelin. </li></ul></ul>
  46. 49. Cardiac Catheterization while undergoing an MI <ul><li> </li></ul><ul><li>Angioplasty and Stenting </li></ul><ul><li> </li></ul>
  47. 50. Coronary artery bypass graft <ul><li>Surgical treatment where saphenous vein is harvested from the lower leg and used to bypass the occluded vessels. </li></ul>
  48. 52. Long Term Care <ul><li>Smoking Cessation and lifestyle modifications. </li></ul><ul><li>Aspirin, Beta Blockers and Clopidogrel will be indefinite. </li></ul><ul><li>Lipid lowering medication along with diet modifications. </li></ul>
  49. 53. References <ul><li>Bolooki, H.M.& Askari, A. (Published August 8 2010). Acute Myocardial Infarction. Retrieved from </li></ul><ul><li>Lewis, S., Heitkemper, M., & Dirksen, S. (2004). Medical surgical nursing assessment and management of clinical problems. St. Louis, MO: Mosby. </li></ul><ul><li>McCance, K.L., Huether, S.E., Brashers, V.L.& Rote, N.S. (2010). Pathophysiology the biological basis for disease in adults and children. Maryland Heights, MO: Mosby Elsevier. </li></ul>